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      Experiences after Twenty Months with Pandemic Influenza A (H1N1) 2009 Infection in the Naïve Norwegian Pig Population

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          Abstract

          Pandemic (H1N1) 2009 influenza A virus was detected in Norwegian pigs in October 2009. Until then, Norway was regarded free of swine influenza. Intensified screening revealed 91 positive herds within three months. The virus was rapidly transmitted to the susceptible population, including closed breeding herds with high biosecurity. Humans were important for the introduction as well as spread of the virus to pigs. Mild or no clinical signs were observed in infected pigs. Surveillance of SIV in 2010 revealed that 41% of all the Norwegian pig herds had antibodies to pandemic (H1N1) 2009 virus. Furthermore, this surveillance indicated that pigs born in positive herds after the active phase did not seroconvert, suggesting no ongoing infection in the herds. However, results from surveillance in 2011 show a continuing spread of the infection in many herds, either caused by new introduction or by virus circulation since 2009.

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          Heterosubtypic immunity to influenza A virus: where do we stand?

          K Grebe, Jack Bennink, Jonathan W Yewdell (2008)
          Influenza A virus (IAV) strains are denoted by the subtype of their hemagglutinin (HA) and neuraminidase (NA) virion surface proteins. Major changes in HA subtype among strains circulating in humans are referred to as "antigenic shift". Antigenic shift can occur by two means: direct transmission of a zoonotic strain to humans or through reshuffling of the segmented genome in cells co-infected with animal and human strains. The lack of circulating anti-HA antibodies in human populations to a novel IAV results in extremely high frequency of illness and the potential for severe morbidity and mortality on a world-wide basis; the dreaded pandemic. Such pandemics could be partially controlled by developing a vaccine that generates effective heterosubtypic immunity (HSI) based on immune recognition of IAV antigens conserved across all viral strains. While it has long been known that T cells exhibit such broad cross-reactive specificity that could provide effective HSI, recent animal studies suggest a potential role for antibodies as well. Here we review current knowledge of the mechanisms contributing to HSI to influenza and speculate on the potential for this approach to contribute to public health.
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            Pathogenesis and transmission of the novel swine-origin influenza virus A/H1N1 after experimental infection of pigs.

            Sasan Fereidouni, Donata Kalthoff, Angele Breithaupt … (2009)
            Influenza virus A/H1N1, which is currently causing a pandemic, contains gene segments with ancestors in the North American and Eurasian swine lineages. To get insights into virus replication dynamics, clinical symptoms and virus transmission in pigs, we infected animals intranasally with influenza virus A/Regensburg/D6/09/H1N1. Virus excretion in the inoculated pigs was detected in nasal swabs from 1 day post-infection (p.i.) onwards and the pigs developed generally mild symptoms, including fever, sneezing, nasal discharge and diarrhoea. Contact pigs became infected, shed virus and developed clinical symptoms similar to those in the inoculated animals. Plasma samples of all animals remained negative for virus RNA. Nucleoprotein- and haemagglutinin H1-specific antibodies could be detected by ELISA 7 days p.i. CD4(+) T cells became activated immediately after infection and both CD4(+) and CD8(+) T-cell populations expanded from 3 to 7 days p.i., coinciding with clinical signs. Contact chickens remained uninfected, as judged by the absence of virus excretion, clinical signs and seroconversion.
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              Replication, Pathogenesis and Transmission of Pandemic (H1N1) 2009 Virus in Non-Immune Pigs

              Sharon M. Brookes, Alejandro Nunez, Bhudipa Choudhury … (2010)
              The declaration of the human influenza A pandemic (H1N1) 2009 (H1N1/09) raised important questions, including origin and host range [1], [2]. Two of the three pandemics in the last century resulted in the spread of virus to pigs (H1N1, 1918; H3N2, 1968) with subsequent independent establishment and evolution within swine worldwide [3]. A key public and veterinary health consideration in the context of the evolving pandemic is whether the H1N1/09 virus could become established in pig populations [4]. We performed an infection and transmission study in pigs with A/California/07/09. In combination, clinical, pathological, modified influenza A matrix gene real time RT-PCR and viral genomic analyses have shown that infection results in the induction of clinical signs, viral pathogenesis restricted to the respiratory tract, infection dynamics consistent with endemic strains of influenza A in pigs, virus transmissibility between pigs and virus-host adaptation events. Our results demonstrate that extant H1N1/09 is fully capable of becoming established in global pig populations. We also show the roles of viral receptor specificity in both transmission and tissue tropism. Remarkably, following direct inoculation of pigs with virus quasispecies differing by amino acid substitutions in the haemagglutinin receptor-binding site, only virus with aspartic acid at position 225 (225D) was detected in nasal secretions of contact infected pigs. In contrast, in lower respiratory tract samples from directly inoculated pigs, with clearly demonstrable pulmonary pathology, there was apparent selection of a virus variant with glycine (225G). These findings provide potential clues to the existence and biological significance of viral receptor-binding variants with 225D and 225G during the 1918 pandemic [5].
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                Author and article information

                Journal
                Journal ID (nlm-ta): Influenza Res Treat
                Journal ID (iso-abbrev): Influenza Res Treat
                Journal ID (publisher-id): IRT
                Title: Influenza Research and Treatment
                Publisher: Hindawi Publishing Corporation
                ISSN (Print): 2090-1380
                ISSN (Electronic): 2090-1399
                Publication date (Print): 2011
                Publication date (Electronic): 3 January 2012
                Volume: 2011
                Electronic Location Identifier: 206975
                Affiliations
                1Department of Laboratory Services, Norwegian Veterinary Institute, P.O. Box 750 Sentrum, 0106 Oslo, Norway
                2Department of Health Surveillance, Norwegian Veterinary Institute, P.O. Box 750 Sentrum, 0106 Oslo, Norway
                3Department of Control, Norwegian Food Safety Authority, Kyrkjevegen 332, 4325 Sandnes, Norway
                4Norwegian Pig Health Service, Animalia, P.O. Box 396 Økern, 0513 Oslo, Norway
                5Division of Infectious Disease Control, Department of Virology, Norwegian Institute of Public Health, P.O. Box 4404 Nydalen, 0403 Oslo, Norway
                Author notes

                Academic Editor: Montserrat Torremorell

                Article
                DOI: 10.1155/2011/206975
                PMC ID: 3447302
                PubMed ID: 23074654
                SO-VID: 829940bb-467f-4349-83f8-536d68ad27e3
                Copyright statement: Copyright © 2011 B. Gjerset et al.
                License:

                This is an open access article distributed under the Creative Commons Attribution License, which permits unrestricted use, distribution, and reproduction in any medium, provided the original work is properly cited.

                History
                Date received : 15 September 2011
                Date revision received : 21 November 2011
                Date accepted : 18 December 2011
                Categories
                Subject: Research Article

                ScienceOpen disciplines: Infectious disease & Microbiology
                Data availability:
                ScienceOpen disciplines: Infectious disease & Microbiology

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